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1 Department of Veterinary Biomedical Sciences and Dalton Cardiovascular Research Center, University of Missouri at Columbia, Columbia, Missouri 65211; and 2 Department of Kinesiology and Department of Anatomy and Physiology, Kansas State University, Manhattan, Kansas 66506
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The effect of thyroid status on arterial baroreflex function and autonomic contributions to resting blood pressure and heart rate (HR) were evaluated in conscious rats. Rats were rendered hyperthyroid (Hyper) or hypothyroid (Hypo) with triiodothyronine and propylthiouracil treatments, respectively. Euthyroid (Eut), Hyper, and Hypo rats were chronically instrumented to measure mean arterial pressure (MAP), HR, and lumbar sympathetic nerve activity (LSNA). Baroreflex function was evaluated with the use of a logistic function that relates LSNA or HR to MAP during infusion of phenylephrine and sodium nitroprusside. Contributions of the autonomic nervous system to resting MAP and HR were assessed by blocking autonomic outflow with trimethaphan. In Hypo rats, the arterial baroreflex curve for both LSNA and HR was shifted downward. Hypo animals exhibited blunted sympathoexcitatory and tachycardic responses to decreases in MAP. Furthermore, the data suggest that in Hypo rats, the sympathetic influence on HR was predominant and the autonomic contribution to resting MAP was greater than in Eut rats. In Hyper rats, arterial baroreflex function generally was similar to that in Eut rats. The autonomic contribution to resting MAP was not different between Hyper and Eut rats, but predominant parasympathetic influence on HR was exhibited in Hyper rats. The results demonstrate baroreflex control of LSNA and HR is attenuated in Hypo but not Hyper rats. Thyroid status alters the balance of sympathetic to parasympathetic tone in the heart, and the Hypo state increases the autonomic contributions to resting blood pressure.
hypothyroidism; hyperthyroidism; sympathetic nerve activity; ganglionic blockade; rats
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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VARIATIONS FROM EUTHYROID STATUS affect virtually all physiological systems, and effects on the cardiovascular system are particularly pronounced. Changes in thyroid status are associated with changes not only in cardiac and vascular function but also in autonomic regulation of the cardiovascular system (14). The clinical picture of hyperthyroidism is suggestive of increased sympathetic activity (1, 14), but assessments of sympathetic activity suggest that sympathetic outflow is either unchanged or reduced (5, 7, 13, 18). In contrast, whereas several clinical features of hypothyroidism are consistent with reduced sympathetic activity, indirect techniques suggest that sympathetic activity is elevated (4, 16, 23). Interestingly, in both hypo- and hyperthyroidism, the influence of the parasympathetic nervous system on heart rate (HR) seems to be reduced (3, 10, 11, 15). The mechanisms for the change in resting levels of sympathetic and parasympathetic outflow are unknown but could be due to a variety of mechanisms, including direct effects (excess or depletion) of thyroid hormone in central regions involved in autonomic regulation or changes in cardiovascular reflex systems that control the autonomic nervous system. Both hypo- and hyperthyroidism are associated with exercise intolerance (19). HR, blood pressure, and skeletal muscle blood flow responses to dynamic exercise suggest hypothyroid animals exhibit blunted activation of the sympathetic nervous system during dynamic exercise (20) and an exaggerated sympathetic response in hyperthyroidism (17, 21). The sympathetic nervous system activation that occurs in response to dynamic exercise requires, in part, participation of the arterial baroreflex (25). The arterial baroreflex tonically influences activity of both the sympathetic and parasympathetic nervous systems and buffers changes in arterial pressure on a beat-to-beat basis. The function of the arterial baroreflex is plastic and can be altered by numerous stimuli including circulating hormones. It is unknown whether arterial baroreflex function is altered by thyroid status. Changes in arterial baroreflex function during either hypo- or hyperthyroidism could potentially account for some of the change in autonomic outflow at rest and for the altered regulation of autonomic function in response to various stresses, including dynamic exercise.
The purpose of this study was to determine whether changes in thyroid status alter arterial baroreflex function. We used well-established rat models of hypo- and hyperthyroidism. Baroreflex responses in lumbar sympathetic nerve activity (LSNA) and HR over a wide range of arterial pressures were evaluated in conscious rats. In addition, studies were conducted to estimate the contribution of the autonomic nervous system to the maintenance of arterial pressure and resting HR by pharmacologically blocking the autonomic nervous system with trimethaphan, a ganglionic blocking agent.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Animals. All procedures were approved by the Institutional Animal Care and Use Committee of the University of Missouri at Columbia. Male Sprague-Dawley rats (Sasco) weighing 175-200 g were housed two per cage under controlled conditions of temperature (20-21°C) and light (12:12-h light-dark cycle). Rats were randomly assigned to one of three groups: euthyroid control (Eut), hypothyroid (Hypo), and hyperthyroid (Hyper). Rats of the Hypo and Hyper groups consumed food ad libitum. Rats of the Eut group were food restricted such that bulk food intake was ~80% of normal to keep their body weights similar among groups.
Treatment. Rats were rendered hypothyroid by 2-3 mo of treatment with propylthiouracil (0.04 g/100 ml; Sigma) in the drinking water, as previously described (20). Hyperthyroidism was induced in rats by intraperitoneal administration of triiodothyronine (300 µg/kg in 0.50 mM NaOH; Sigma) on alternate days over 2-3 mo (21).
Determination of treatment efficacy. Establishment of altered thyroid status was confirmed by assessing left ventricular weight and soleus muscle oxidative capacity. The latter was estimated by determining activity of citrate synthase, a marker enzyme for oxidative metabolism, with the use of the colorimetric assay of Srere (28). It is well established that hypothyroidism induces a reduction in skeletal muscle citrate synthase activity (6, 9, 20). In contrast, hyperthyroidism is associated with an increase in muscle citrate synthase activity as well as left ventricular hypertrophy (6, 9, 21).
Surgical procedures. After the 2- to 3-mo treatment or control period, each rat was instrumented with catheters and nerve electrodes. All surgical procedures were performed using aseptic technique under halothane anesthesia. Catheters (polyethylene-10 fused to polyethylene-50) were inserted into the aorta and abdominal vena cava via the femoral artery and vein. Catheters were filled with heparinized saline (10 U/ml) and capped with an airtight plug. Through a midline abdominal incision, electrodes were implanted on the lumbar sympathetic chain caudal to the left kidney. Nerves and electrodes were covered with a polyvinylsiloxane gel (Coltene President), which was allowed to harden before closure. The electrodes were manufactured using Teflon-insulated silver wires (0.005-in. diameter; Medwire) threaded through Silastic tubing (0.025-in. inner diameter). A ground wire was sewn to the surrounding muscle tissue. The catheters, electrodes, and ground wire were tunneled subcutaneously and exteriorized in the dorsal cervical region.
After the surgical procedures were completed, animals were given 30 ml of saline subcutaneously to aid in volume restoration. After animals had recovered from anesthesia, they were returned to their cage for a ~24-h recovery period before the start of any experimental procedures. By the end of the recovery period, the animals were grooming normally and displayed normal cage activity.Experimental procedures. On the day of the experiment, the animal was placed in an experimental cage that was furnished with the animal's own bedding. The experimental cage was placed within a Faraday cage. The arterial catheter was attached to a pressure transducer for recording arterial pressure. Mean arterial pressure (MAP) was derived electronically using a low-pass filter. HR was determined from pulsatile arterial pressure by a cardiotachometer. LSNA was amplified 1,000 times with the use of a preamplifier (Grass P511) and filtered using a high-pass frequency level of 30 Hz and a low-pass frequency level of 3 kHz. Action potentials were monitored with an oscilloscope (Tektronix) and an audio monitor (Grass M8). Nerve activity was rectified and integrated using a root-mean-square converter with a time constant of 28 ms. The rectified integrated signal was averaged electronically. The background noise level of the nerve recording was determined as the minimum value during maximal elevation in arterial pressure. Audio and visual monitoring of nerve activity during this period was utilized to verify that sympathetic nerve activity bursts were eliminated. LSNA was defined as the amount of recorded nerve activity after subtraction of background noise.
Experimental protocol.
Baseline hemodynamic parameters were recorded for ~30 min to allow
stabilization of MAP, HR, and LSNA before the start of the experimental
protocol. The animals were resting quietly in their cages during the
experimental procedures. Although the electrocardiogram was not
recorded in these experiments, no signs of obvious arrhythmia were
observed. Arterial baroreflex curves were generated by producing ramp
changes in arterial pressure and recording the reflex changes in HR and
LSNA. Ramp increases in arterial pressure were produced over 2-3
min by continuous intravenous infusion of the
1-adrenergic agonist phenylephrine (PE) at progressively
increasing rates (2-25 µg · kg
1 · min1).
Hemodynamic parameters were allowed to recover to within 10% of
starting values (~20 min). Arterial pressure then was decreased (to ~40 mmHg) in a ramp fashion over 2-3 min by continuous
intravenous infusion of sodium nitroprusside (SNP) at progressively
increasing rates (10-100
µg · kg1 · min1). The
rate of change of arterial pressure was held constant by observing the
pressure change and varying the infusion rate. The rate of change
(~1-2 mmHg/s) was similar across all animals. This methodology
was used to allow evaluation of both sympathetic and parasympathetic
nerve activity effects and to prevent resetting of the arterial
baroreflex (29). To minimize any potential effects of
released humoral agents (e.g., angiotensin II, vasopressin, etc.) on
baroreflex function, baroreceptors were activated (PE infusion) before
being unloading (SNP infusion).
80°C for later analysis of citrate synthase activity. The rats were
euthanized with an overdose of pentobarbital sodium. The heart was
removed, and the left ventricle was isolated and weighed.
Data analysis. All data are expressed as means ± SE.
LSNA was expressed and analyzed as a percentage of the control level of LSNA before changing arterial pressure (%Baseline). The control level of LSNA was defined as 100%. In addition, LSNA was analyzed relative to the maximum recorded level of LSNA during a decrease in MAP. In this case, the maximum recorded level of LSNA was defined as 100% (%Peak). Arterial baroreflex curves were generated by relating HR and LSNA to MAP. The data were fit to a sigmoidal logistic function (12) with the use of a standard software package (SigmaPlot for Windows, Jandel Scientific; San Rafael, CA). The following equation was used to fit the data
![SNA or HR<IT>=</IT>(<IT>P<SUB>1</SUB>−P<SUB>4</SUB></IT>)<IT>/</IT>{<IT>1+e</IT><SUP>[<IT>P<SUB>2</SUB></IT>(MAP<IT>−P<SUB>3</SUB></IT>)]</SUP>}<IT>+P<SUB>4</SUB></IT>](/content/vol280/issue5/fulltext/H2061/img001.gif)
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(1) |
![G<SUB>MAP</SUB><IT>=</IT>−(<IT>P<SUB>1</SUB>−P<SUB>4</SUB></IT>)<IT>P<SUB>2</SUB>×e</IT><SUP><IT>P<SUB>2</SUB></IT>(MAP<IT>−P<SUB>3</SUB></IT>)</SUP><IT>/</IT>[<IT>1+e</IT><SUP><IT>P<SUB>2</SUB></IT>(MAP<IT>−P<SUB>3</SUB></IT>)</SUP>]<SUP><IT>2</IT></SUP>](/content/vol280/issue5/fulltext/H2061/img002.gif)
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(2) |
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Treatment efficacy.
Treatment with propylthiouracil was effective in establishing a
hypothyroid state. Body weight, left ventricular weight, and soleus
muscle citrate synthase activity were lower in Hypo rats compared with
Eut rats (Table 1). Conversely, increased
left ventricular weight, left ventricular-to-body weight ratio, and soleus muscle citrate synthase activity were exhibited by Hyper animals
(Table 1). Food restriction of the Eut animals was effective in
maintaining similar body weights between the Eut and Hyper rats. The
Hypo rats failed to gain weight at the same rate as the Eut rats, which
resulted in lower body weights in the Hypo animals.
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Baroreflex control of LSNA.
The effect of altered thyroid status on arterial baroreflex control of
LSNA analyzed as a percentage of control LSNA (%Baseline) is presented
in Fig. 2. As indicated in Table 1, Hypo
rats had a lower baseline MAP compared with Eut or Hyper animals (Fig. 2A). The gain of the baroreflex curves as a function of MAP
is presented in Fig. 2B. All groups exhibited reflex
increases and decreases in LSNA in response to decreases and increases
in MAP, respectively. Baroreflex control of LSNA in Hyper rats was
similar to Eut rats over the range of arterial pressure evaluated (Fig. 2A). The maximum and minimum LSNA, pressure at the midpoint
of the curve, and peak gain of the Hyper and Eut rats were not
statistically different (Table 2). The
gain of baroreflex control of LSNA specifically over a pressure range
of 75-95 mmHg was greater in the Hyper rats compared with the Eut
rats (Fig. 2B). In contrast, Hypo rats exhibited severe
blunting of arterial baroreflex function. The ability to increase LSNA
in response to decreases in MAP was markedly blunted in Hypo rats
compared with Eut rats (Fig. 2A). The maximum LSNA attained
during decreases in MAP was significantly attenuated in Hypo rats
compared with Eut and Hyper groups (Table 2). The blunted
sympathoexcitatory response in Hypo rats was significant at arterial
pressures <75 mmHg. In addition, the Hypo rats had a significantly
reduced gain compared with Eut rats from pressures of 60-90 mmHg
(Fig. 2B). Neither the midpoint of the curves nor the
minimum level of LSNA was different among the three groups (Table 2).
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Baroreflex control of HR.
The effect of altered thyroid status on arterial baroreflex control of
HR is presented in Fig. 3. As indicated
in Table 1, resting MAP was lower in Hypo rats compared with Eut or
Hyper animals, but baseline HR was similar among groups (Fig.
3A). All groups exhibited reflex increases and decreases in
HR in response to changes in MAP (Fig. 3A). The gain of the
baroreflex curves as a function of MAP is presented in Fig.
3B. Baroreflex control of HR in Hyper rats was similar to
that in Eut rats over the range of arterial pressures evaluated. In
addition, the gain of the baroreflex curve in the Hyper animals was not
significantly different from that of the Eut rats. The maximum HR,
minimum HR, pressure at the midpoint of the curve, or peak gain were
not different between the Hyper and Eut rats (Table
4). In contrast, Hypo rats exhibited a
markedly altered baroreflex control of HR. In Hypo rats, HR was reduced
over the complete range of pressures, resulting in a downward shift in
baroreflex control of HR (Fig. 3A). The resting HR of the
Hypo rats was close to the maximum HR of their baroreflex curve,
demonstrating that the Hypo rats had a limited ability to increase HR
when arterial pressure was decreased. In the Hypo rats, both the
maximum and the minimum HR were decreased compared with Eut and Hyper
groups (Table 4). Neither the midpoint of the curves nor the peak gain
were different among the three groups (Table 4). The gain of baroreflex
control of HR in Hypo rats was blunted significantly compared with that
in the Eut animals over a pressure range of 60-85 mmHg but was
enhanced through pressures of 100-115 mmHg (Fig. 3B).
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Response to autonomic blockade.
The average MAP and HR values before and after autonomic blockade with
trimethaphan in Eut, Hypo, and Hyper rats are presented in Fig.
4. The maximum changes in MAP and HR in
response to trimethaphan are presented in Fig.
5. Before autonomic blockade, baseline
MAP and HR in the Hypo and Hyper groups were not different from the Eut
group, although MAP in the Hypo group tended to be lower (Fig. 4, open
bars). Autonomic blockade by intravenous administration of trimethaphan
decreased MAP in all groups (Figs. 4A and 5A). The absolute level of MAP after autonomic blockade was similar in Eut
and Hyper animals; however, pressure was lower in the Hypo rats
compared with the Eut or Hyper animals (Fig. 4A, solid
bars). In a similar fashion, the reduction in MAP in response to
ganglionic blockade (Fig. 5A) was similar in Eut and Hyper
animals. However, the depressor response to trimethaphan was greater in
the Hypo group compared with the other groups. The greater depressor
response in Hypo animals occurred despite a lower baseline MAP in the
Hypo animals.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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These studies evaluated the effect of thyroid status on arterial baroreflex control of LSNA and HR in conscious rats. The major findings of this study are that Hypo rats exhibit blunted baroreflex mediated increases in LSNA and HR and a downward shift in baroreflex control of HR compared with Eut rats. In contrast, baroreflex function generally was similar in Hyper and Eut rats. These studies also evaluated the autonomic contributions to resting arterial pressure and HR. In Hyper and Eut rats, autonomic blockade produced a similar decrease in MAP, but Hyper rats had a greater increase in HR than Eut rats. Hypo rats exhibited a greater fall in both MAP and HR than Eut rats after autonomic blockade. Taken together, the data indicate that Hypo rats have depressed arterial baroreflex function and elevated dependence on resting sympathetic tone to both the heart and vasculature. Hyper rats exhibit normal baroreflex function and normal sympathetic tone to the vasculature.
Evidence of altered thyroid state. Propylthiouracil treatment and administration of triiodothyronine in rats has been utilized previously by numerous laboratories to induce a hypothyroid and hyperthyroid state, respectively (6, 20, 21, 24). In this study, Hypo rats had reduced weight gain, left ventricular weight, soleus muscle citrate synthase activity, and a decrease in intrinsic HR, which indicated that propylthiouracil was effective in producing hypothyroidism. In contrast, regular administration of triiodothyronine produced cardiac hypertrophy, increased soleus muscle citrate synthase activity, and an increase in intrinsic HR. These changes are consistent with reported effects of altered thyroid status in rats (6, 20-22) and suggest that the Hypo and Hyper rats in this study were hypothyroid and hyperthyroid, respectively.
Effect of thyroid status on arterial baroreflex function. In this study, several significant changes in arterial baroreflex function were observed in Hypo rats compared with Eut rats. Hypo rats exhibited a blunted sympathoexcitatory response to low arterial pressures. This reduced capacity to reflexly increase LSNA was demonstrated whether the curve relating LSNA to MAP was calculated as a percentage of baseline or of maximum LSNA. In addition, baroreflex control of HR was shifted downward, and resting HR in Hypo rats was near the upper plateau of the curve. Thus the Hypo rats were limited in their ability to increase HR and LSNA in response to decreases in MAP. These changes in baroreflex control of LSNA and HR occurred in the absence of any shifts in the midpoint of the curves, suggesting that there was no significant pressure resetting of the baroreflex in the Hypo rats. Conversely, Hypo rats responded to increases in arterial pressure with similar sympathoinhibitory and bradycardic responses compared with Eut rats. Although the peak gain of either the LSNA or HR baroreflex curve was not different, the Hypo rats exhibited a decreased gain close to resting arterial pressures compared with the baroreflex gain of the Eut rats. These data suggest that Hypo rats have a blunted arterial baroreflex; specifically, they exhibit impaired ability to increase sympathetic activity and HR to hypotensive challenges.
In Hyper rats, the major indexes (maximum, midpoint, minimum, and peak gain) used in this study to describe arterial baroreflex function were not altered. Hyper rats did exhibit a slightly enhanced gain compared with Eut rats only over a specific segment of the range of MAP (75-95 mmHg) used to generate the LSNA baroreflex curve. Taken together, these data suggest that Hyper rats generally have similar arterial baroreflex function compared with Eut rats. It has been demonstrated that extreme food restriction in middle-aged Fischer 344 rats enhances baroreflex control of HR and produces a substantial resting bradycardia (8). The major change in the reflex control of HR was a greater tachycardic response to decreases in arterial pressure. In these Fischer rats, body weight was reduced ~45% compared with the control group by the 10-12 mo of reduced calorie diet (~60% of control group). Furthermore, excessive calorie intake has been shown to blunt arterial baroreflex function (2). In the current study, the Eut rats were food restricted ~20% for the 2- to 3-mo treatment protocol, which kept the body weights of the Eut and Hyper rats similar. It is possible that this level of food restriction would alter arterial baroreflex function; however, this seems unlikely because the magnitude and duration of the food restriction was much less than previously studied (8).Autonomic contributions to arterial pressure and HR. In this study, Hypo rats had a greater autonomic contribution to resting MAP compared with Eut rats. Also in Hypo rats HR decreased in response to ganglionic blockade, suggesting a predominant sympathetic influence on HR at rest. The lower residual MAP after ganglionic blockade could be due to a variety of mechanisms in the Hypo rats including reduced resting tone of resistance vessels, lower cardiac output, or lower circulating levels of vasoconstrictor hormones, including angiotensin II or vasopressin. The enhanced autonomic contribution to MAP is consistent with enhanced dependency on sympathetic tone to the vasculature and heart. However, the data from this study do not directly address this concept. It is difficult to directly compare resting levels of sympathetic outflow between different groups of animals. Keeping this technical limitation in mind, the concept of increased sympathetic outflow is consistent with previous studies (4, 13, 16) that measured plasma catecholamines and norepinephrine turnover rates in hypothyroidism. In the Hypo rats, the sympathetic influence on resting HR compensated for the lower intrinsic HR of the Hypo rats (22) and normalized the resting HR to a similar rate as the Eut rats. In contrast, the increased autonomic contributions to resting MAP in the Hypo rats were not able to fully compensate, and MAP was decreased compared with the Eut rats.
The Hyper rats had similar autonomic contributions to resting MAP as the Eut rats. These data are supported by previous studies (5, 7, 13) that directly or indirectly measured sympathetic outflow. In Hyper rats, ganglionic blockade increased HR, suggesting a predominant parasympathetic influence on resting HR that apparently balanced the elevated intrinsic HR in Hyper rats. The increase in intrinsic HR likely is due to direct effects of thyroid hormone on the heart (13, 22, 26, 30). The specific mechanism for increases in vagal influence on HR is unknown and could be due to an increase in vagal nerve activity, an increase in acetylcholine release, enhanced muscarinic receptor/signaling pathway, or a combination of any of these possibilities.Perspectives. The specific physiological consequences of blunted arterial baroreflex function in Hypo rats are unknown. It would be predicted that Hypo rats would have a reduced capacity to maintain blood pressure in situations that require reflex activation of the sympathetic nervous system such as hemorrhagic stress, orthostatic stress, and dynamic exercise. It is well documented that hypothyroidism results in exercise intolerance with decreases in both maximal oxygen uptake and endurance (19). The mechanisms that account for the reduced exercise tolerance are multifactorial, but the alteration in baroreflex function may be a contributing factor. It has been suggested that inadequate cardiovascular support accounts for a majority of the exercise intolerance in hypothyroidism (19). Although direct changes in cardiac and vascular function due to the deficiency in thyroid hormone must play a role in the exercise intolerance, the effects of sympathetic nervous system activation during dynamic exercise in hypothyroidism also are reduced compared with the euthyroid state (19). Because the normal sympathoexcitatory response to dynamic exercise is dependent at least in part on arterial baroreflex function (25), one possibility is that the blunted baroreflex function in Hypo rats accounts for part of the inadequate cardiovascular response during dynamic exercise. Hyperthyroidism also is associated with a decrease in exercise tolerance. In contrast to the inadequate cardiovascular support observed in hypothyroidism, altered energy metabolism within the exercising muscle accounts for the majority of the reduced exercise tolerance in hyperthyroidism (19). The sympathetic response to dynamic exercise is appropriate or potentially enhanced in hyperthyroidism (7, 19). The relatively unchanged baroreflex function in Hyper rats is consistent with the sympathetic response to dynamic exercise in the hyperthyroid state. Future studies that evaluate baroreflex function during exercise in hyperthyroidism and hypothyroidism are necessary to test these ideas directly.
In conclusion, Hypo rats exhibit altered arterial baroreflex function and, specifically, have a reduced capacity to increase LSNA and HR in response to decreases in arterial pressure. In addition, Hypo rats have a greater dependence on autonomic contributions to resting blood pressure and HR, consistent with an elevation in baseline sympathetic tone. The intrinsic HR of Hypo rats was reduced compared with that in Eut rats. In contrast, baroreflex control of LSNA and HR generally was similar between Hyper and Eut rats. The autonomic contribution to resting MAP was also similar between Hyper and Eut rats, but the Hyper rats appeared to have a predominant vagal influence on HR that counterbalanced the increase in intrinsic HR seen with hyperthyroidism. Taken together, these data suggest that hypothyroidism in rats blunts the arterial baroreflex and alters the relative contribution of systems that maintain resting blood pressure and HR. In contrast, hyperthyroidism in rats produces few quantitative effects on the baroreflex and on the contribution of the autonomic nervous system to the maintenance of resting arterial pressure.| |
ACKNOWLEDGEMENTS |
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The authors thank Sarah A. Friskey and Jodie A. Smith for excellent technical assistance in performing the surgical preparations and experimental procedures. The authors also thank Tammy Strawn for performing the citrate synthase activity assays.
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FOOTNOTES |
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This research was supported by National Heart, Lung, and Blood Institute Grants HL-55306, HL-36088, and HL-57226, by the Missouri Affiliate of the American Heart Association, and by the University of Missouri Research Board.
Address for reprint requests and other correspondence: E. M. Hasser, Dalton Cardiovascular Research Center, 134 Research Park Dr., Univ. of Missouri, Columbia, MO 65211-3300 (E-mail: HasserE{at}missouri.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 7 August 2000; accepted in final form 15 December 2000.
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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statistically different from peak
response of Eut rats, and 
statistical difference between peak
response of Hypo and Hyper rats at P < 0.05.
